Ischemic colitis associated with acute carbon monoxide poisoning

To the Editor:

Our hospital initiated a prospective, protocolized follow-up programme of acute carbon monoxide (CO) poisonings in 1996 (1). Since then until December 2006, 945 patients with CO poisoning have been attended (2). It is known that the clinical manifestations of CO poisoning are variable and non-specific (3). A specific follow-up programme of patients intoxicated by CO allows infrequent presentations to be detected. We present the case of a patient who developed ischemic colitis following CO exposure.

An 87-year-old woman with a history of adenocarcinoma of the cecum, who underwent a right hemicolectomy 20 months before, was admitted to the Emergency Department due to reduced consciousness (Glasgow Coma Score = 12), headache, and vomiting. The patient had been exposed to CO produced by a malfunctioning propane gas heater for about 60 minutes. She was taking no medications. The examination was unremarkable. Thirty minutes after the CO exposure, her haemoglobin (Hb) was 11.7 g/dL and carboxyhaemoglobin (COHb) was 19.7%. An electrocardiogram (ECG) showed sinus rhythm and a 2 mm depression in the ST segment with a negative T wave in II, III, aVF, and V3-V6. Serial cardiac enzymes and the chest X-ray were normal and the ECG was normal 6 hours later. The initial symptoms disappeared rapidly with 100% oxygen and fluids. No other drugs or therapy were adminstered. However, 30 minutes after Emergency Department admission, the patient complained of diffuse abdominal pain and there was abundant blood in the feces; the blood pressure was normal. The Hb level was 10.4 g/dL four hours later. A colonoscopy showed mucosa with edema, erythema, submucous haemorrhages and superficial longitudinal ulcerations in a 10 cm portion of the sigmoid colon, which were compatible with ischemic colitis. A biopsy of the mucosa showed detachment of a large part of the epithelium with loss of glands and hemorrhagic regions in the lamina propia. The stool culture was negative and consumption of vasoactive substances was ruled out. The clinical course was favourable and the abdominal pain and bloody stool remitted with symptomatic treatment. There were no manifestations of delayed neuropsychiatric syndrome.

CO poisoning is a known cause of hypoxic injury of the central nervous system and the myocardium (4,5). The main manifestations of the case presented here were changes in the ECG and gastrointestinal haemorrhage. The time sequence of the clinical course and the absence of another cause suggest that the ischemic colitis may have been due to anoxia in the intestinal mucosa secondary to CO poisoning. To date, only two cases of intestinal ischemia secondary to CO poisoning and only one with concurrent coronary and intestinal involvement have been described (6,7). Balzan et al. reported a patient with CO poisoning treated with hyperbaric oxygen who presented an acute coronary syndrome with acute pulmonary oedema complicated by a massive, fatal mesenteric ischemia (6). The other reported case had abdominal pain and bloody diarrhea as manifestations of mesenteric ischemia and also presented hepatic and renal failure (7). Both cases were associated severe CO poisoning, with COHb levels higher than those of our patient (45 and 34%, respectively) and multiorgan involvement. Our patient presented moderate CO poisoning (COHb 19.7%) in which intestinal ischemia of the sigmoid colon was confirmed by clinical, endoscopic and histologic criteria (8).

In our case, the use of hyperbaric therapy was rejected due to the appearance of severe gastrointestinal haemorrhage which led to initial suspicions of a recurrence of the tumour and because the nearest hyperbaric chamber is 4 hours from our hospital.

Ischemic colitis is the most-frequent form of mesenteric ischemia. Ischemic lesions of the colon are due to the hypoxia, which causes detectable injury in the superficial part of the mucosa within one hour (9,10). In CO poisonings, tissue hypoxia is due to competitive bonding of CO to the heme group of hemoglobin, from where it displaces oxygen and to the bonding of CO with mitochondrial cytochrome c oxidase, directly interfering with cellular respiration (3,4). Our case suggests that hypoxia can affect the intestine in addition to the central nervous system and the heart. In conclusion, we report a case of ischemic colitis associated with carbon monoxide poisoning.